Role of nitric oxide in short-term potentiation and long-term facilitation: involvement of NO in breathing stability.

Role of nitric oxide in short-term potentiation and long-term facilitation: involvement of NO in breathing stability.
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一氧化氮在短期增强和长期促进中的作用:一氧化氮参与呼吸稳定性。

DOI:
10.1007/978-1-4615-1375-9_33
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发表时间:
2001
影响因子:
--
通讯作者:
Prabhakar,NR
Prabhakar,NR
中科院分区:
医学4区
文献类型:
--
作者:
Kline,DD;Prabhakar,NR

文献摘要

相似文献

有充分证据表明,不同物种对各种刺激的呼吸增加通常可能比实际刺激持续时间更长(参见参考文献 1、2)。例如,在短暂的缺氧挑战后,通气量会在几分钟内缓慢恢复到基线值,这种现象通常被称为“短期增强(STP)”。另一方面,在反复发生缺氧挑战后,根据物种的不同,呼吸可能会在炎热的情况下保持升高状态。反复出现缺氧后这种长期持续的呼吸增强被称为“长期促进(LTF)”。有人提出,STP 和 LTF 对于维持呼吸稳定性至关重要,特别是在涉及动脉血气急剧变化的情况下2,并且可能涉及脑干神经元1,2。最近对海马神经元的研究表明,一氧化氮 (NO) 对于与学习和记忆相关的长时程增强 (LTP) 的发展至关重要3,4。鉴于 NOS-1(产生 NO 的酶)与中缝神经元 5、6 中的 5-HT 共定位,这已被证明对 LTF2 的产生很重要,以及我们最近观察到 NOS-1 突变小鼠在缺氧期间表现出呼吸不稳定 7,促使我们检查 NOS-1 产生的 NO 是否在 STP 和/或 LTF 的发育中发挥作用。
It has been well documented that increases in breathing in response to a variety of stimuli may often outlast the actual period of stimulation in various species (see references1, 2). For instance, after a brief hypoxic challenge, ventilation slowly returns to baseline values over a period of minutes, a phenomenon often termed as “short-term potentiation (STP).” On the other hand, after episodes of recurrent hypoxic challenges, depending on species, breathing may remain elevated as long as an hotir. This long lasting enhancement of respiration that follows recurrent episodes of hypoxia is referred to as “long-term facilitation (LTF).” It has been proposed that STP and LTF are critical for maintaining stability of breathing, especially in situations involving acute changes in arterial blood gases2, and may involve brainstem neurons1,2. Recent studies on hippocampal neurons suggest that nitric oxide (NO) is critical for the development of long term potentiation (LTP) associated with learning and memory3,4. Given that NOS-1, the enzyme that generates NO, is co-localized with 5-HT in raphe neurons5, 6, which has been shown to be important for the generation of LTF2, as well as our recent observation that NOS-1 mutant mice exhibit breathing instability during hypoxia7, prompted us to examine whether NO generated by NOS-1 plays a role in the development STP and/or LTF.